THE PATHOLOGY OF SPAVIN 



S. A. GOLDBERG 

(Department of Comparative Pathology and Bacteriology, New York State Veterinary 
College at Cornell University) 

(A Thesis presented to the Faculty of the Graduate School at Cornell University for 
the Degree of Doctor of Philosophy, September, 1917) 



Reprinted from 

The Journal of Medical Research, Volume XXXVIII., No. a 

(New Series, Vol. XXXIII., No. a), pp. 225-265, May. 1018 



BOSTON 

MASSACHUSETTS 

U.S.A. 



THE PATHOLOGY OF SPAVIN 



A THESIS 



PRESENTED TO THE FACULTY OF THE GRADUATE SCHOOL 
OF CORNELL UNIVERSITY FOR THE DEGREE OF 

DOCTOR OF PHILOSOPHY 



BY 



SAMUEL A. GOLDBERG, A.M., D.V.M. 



Reprinted from The Journal of Medical Research, Volume XXX VIII. No 2 (New Series. 
Vol. XXXIII, No. 2). pp. 225-265, May. 1918. 






&<- 



61921 




THE PATHOLOGY OF SPAVIN.* 

S. A. Goldberg. 
{Department of Comparative Pathology and Bacteriology, Nezo York State 

Veterinary College at Cornell University.) 

{A Thesis presented to the Faculty of the Graduate School at Cornell University for the 

Degree of Doctor of Philosophy, September, iqiy.) 

The term spavin apparently had its origin from the Latin 
spavenius used by Jordanus,Ruffus in the middle of the thir- 
teenth century. Originally it indicated various pathological 
processes in the neighborhood of the tarsal joint. Later there 
were added modifying terms to designate different changes 
in the joint so that the terms bog, blood, or moist spavin 
were used in cases of a fluctuating swelling, the terms 
dry or bone spavin to indicate a hard swelling, ana the term 
occult spavin as an invisible affection of the hock joint. 

The classification of spavin was confusing at one time. De 
Solleysel used the term dry spavin for lameness resembling 
spavin lameness. True spavin he named ox spavin. Saunier 
introduced the term muddy spavin, usually, occurring in 
horses raised in damp, marshy localities. Gibson selected 
the term bone spavin, which Bourgelat named callous spavin. 
By the term dry spavin he understood muscular and neuro- 
pathic lameness. 

Up to the beginning of the nineteenth century the knowl- 
edge of the pathology of spavin was based on various theo- 
ries that were in harmony with the medical view at that time, 
that of humoral pathology. In general, they correspond 
more or less closely with Gibson's idea that spavin begins by 
a soaking of the ligaments with moisture which condenses, 
forming a swelling composed of hardened glue, which later 
grows like the callus of a fractured bone, resembling a piece 
of flint without any visible pores, except the foramina for the 
passage of nerves and blood vessels such as are found in other 
bones that compose the skeleton. 

* Received for publication Feb. 12, 1918. 
(225) 



226 GOLDBERG. 

Haveman in 1805 was the first to show that in spavin the 
articular surfaces are diseased. He wrote, "The cause of 
lameness lies in the articular surfaces. The lameness begins 
as soon as the articular surfaces of the flat bones become 
denuded of cartilage. This is followed by a sort of growing 
together of the bones." He distinguished between the hard 
or bone spavin, the soft or moist spavin, and the occult or 
invisible spavin. 

In 1850 Hertwig brought out the fact that in most instan- 
ces spavin begins as a chronic osteitis and only rarely as an 
acute inflammation of the ligaments and bone caused by 
external injuries. 

Thirty years later Gotti concluded that spavin originates 
in the bones of the hock joint. He found that the process 
usually begins with a very slow osteitis of the central and 
third tarsus and of the metatarsus. In the course of this 
osteitis there is a widening of the Haversian vessels, causing 
a nutritive disturbance of the bony connective tissue. The 
latter is finally transformed into plastic marrow tissue which 
produces a decalcification of the bone. The osteitis later 
leads to a chondritis characterized by a slow and continued 
inflammation of the articular cartilage, accompanied by active 
proliferation and destruction of the ground substance. 

In the inflammatory process of the bone, Gotti recog- 
nized two stages. A destructive period, during which the 
newly formed marrow tends to spread slowly, and a regen- 
erative period during which the newly formed marrow tends 
to be transformed into compact connective or bony tissue. 
Should the proliferating process reach the articular surfaces, 
it is possible for the marrow elements to be transformed 
into osseous tissue and lead to a true ankylosis. 

He considered the formation of osteophytes as secondary, 
usually following the disorder of the joint, and developing 
at the time when the changes have reached the margin of 
the articular surfaces. 

This view that spavin begins in the subchondral bone was 
confirmed by Eberlein, and it is accepted by most veter- 
inarians to-day. Williams claims that spavin is a local 



THE PATHOLOGY OF SPAVIN. 227 

manifestation of a general disease, and some French authors 
(Kitt) claim that the diseases through which young animals 
pass predispose them to this condition. 

Cases. 

The discussion in this paper is based upon a study of 
sixty-five cases of spontaneous inflammations of joints 
leading to the changes described as spavin. In all cases the 
gross appearance was carefully studied and microscopic 
sections were taken from various parts of the joints. On 
account of the necessity of shortening this article a number 
of the cases were eliminated. In these cases the changes 
were similar to those described here, so that they did not add 
materially to the discussion. 

Case 3. — Hock joints from a pure bred percheron foal that died during 
delivery. 

The right hock joint contained a small amount of yellowish synovia. 
The capsule was of normal thickness. The synovial membrane was 
covered in places by fine, reddened, villous tufts. The edges of the 
tibial and astragalar articular surfaces were covered in places by a reticu- 
lum of blood vessels emanating from the synovial membrane, and 
extending into the joint for a distance of four millimeters. This growth 
was readily removed, leaving the underlying cartilage smooth. The 
deeper parts of the articular cartilages were, however, vascularized in 
places. This vascularization extended from the subchondral bone. 

In the remaining articulations of the hock joint the synovial membranes 
were covered by fine, reddened villous tufts. The interosseous ligaments 
were edematous. There were reticular growths of vascular tissue, cover- 
ing the articular cartilages around the interosseous ligaments emanating 
from the surface of the interosseous ligaments, and extending into the 
articulation for a distance of three millimeters. The thickest growth 
was in the articulation between the third tarsus and the metatarsus. All 
the cartilages were of a bluish color and free from erosions. All the 
bones of the hock joint were congested throughout. 

The changes in the left hock joint were similar to those of the right 
hock joint, and similarly located. 

This is evidently a case of subacute proliferative synovitis and an 
erosive osteoarthritis arising from both the bone and the synovial 
membrane. 

The cause was probably an intra-uterine hematogenic infection. 



228 GOLDBERG. 

Case 4. — A full grown fetus removed from a five-year-old cow that died 
of septicemia, following traumatic gastritis. 

The synovial membranes of nearly all the joints were hyperemic. In 
the left hock joint the synovia was reddened, and the cartilages were of a 
bluish color. In the tibio-astragalar articulation the cartilages of both the 
tibia and the astragalus were covered at the periphery by reticular vascular 
growths emanating from the synovial membrane, and extending into the 
joint for a distance of four millimeters. 

The right hock joint showed changes similar to those of the left, 
excepting the synovia was yellowish. 

The joint lesions in the cow were as follows : In the hock joints there 
were yellowish erosions in the tibiae, and on the corresponding astragalar 
articular surfaces. In the stifle joints the synovia contained yellowish 
flocculi. There were several petechiae in the synovial membranes and 
whitish calcified points in the cartilages. The cartilage of the anterior 
and lower ends of the femurs was soft and roughened. There were no 
villous tufts on the synovial membranes. 

In the fetus the case is apparently similar, but not so far advanced as 
Case No. 3. In the cow there is apparently a sero-fibrino-hemorrhagic 
synovitis and a degenerative arthritis, perhaps resulting from the traumatic 
gastritis or of an independent infection. 

In the hock joints there is either a chronic erosive arthritis, or a vestige 
of a previous arthritis. 

Case 5. — A bay foal that died of a pyemia with multiple abscesses of 
the kidneys and diffuse hemorrhage of the adrenals, at the age of thirty- 
six hours. 

In all the joints the synovial membranes were reddened, and the carti- 
lages were of a bluish color. The synovia was of a brownish yellow 
color. 

In the hock joints there were changes similar to those found in the 
other joints of the body. In addition there was a thickening of the 
cartilage in the center of each tibial trochlear ridge. This thickening 
appeared white, while the rest of the articular cartilage was bluish. 

Microscopically, the thickened area was composed of a non-vascular 
reddish material, probably fibrin containing numerous fibroblasts, with 
here and there an island of cartilage. On the surface it was covered by 
cuboidal mesothelial cells. In places it was separated from the articular 
cartilage. These places were lined by cells resembling flattened epithe- 
lium. The cartilaginous matrix of the upper layers of the cartilage were 
stained pinkish, while that of the lower layers took a bluish stain. The 
cartilage contained numerous highly congested capillaries emanating from 
the subchondral bone (Fig. 1). 

In the subchondral bone the marrow spaces were greatly enlarged at 
the expense of the bony trabecular. They contained numerous congested 
blood vessels surrounded by fibroblasts and some marrow cells. These 



THE PATHOLOGY OF SPAVIN. 22p 

consisted of lymphocytes, fat cells, polymorphonuclear leucocytes, 
eosinophiles, eosinophilic myelocytes, with here and there a giant cell. 

Cultures taken from the joints and from other organs showed a growth 
of a short, thick, non-motile, rod-shaped organism in pure culture. The 
colonies were grayish white, rounded, very viscid, and the center was 
nucleated. It produced acid and no gas in dextrose, lactose, and saccha- 
rose bouillon. 

It did not coagulate milk or liquefy blood serum. There was no 
growth on gelatin at room temperature. 

This is apparently a case of acute erosive osteoarthritis of a hema- 
togenic origin, caused by infection. 

Case 7. — Two black and white holstein heifer calves received for diag- 
nosis. One was about two weeks, the other about four weeks old. They 
showed symptoms of white scours and died from a septicemia of B. coli. 

In the younger calf there was subcutaneous edema and hemorrhage 
around both hock joints. In the anterior part of the astragalar trochlear 
grooves there were masses of reddened fibrin. Under the fibrin there was 
a large red erosion in each astragalus. Around this area the cartilage was 
becoming vascularized from the subchondral bone. 

Microscopically, in the most affected portion the cartilage was entirely 
absent. In place of it there was a layer of connective tissue with con- 
gested blood vessels coming from the subchondral marrow. This was 
covered by fibrin containing red corpuscles and a few leucocytes. Towards 
the periphery the cartilage was partly gone and the remaining cartilage 
was covered by an exudate of fibrin and red cells. Farther away the 
cartilage was being vascularized from the subchondral bone. 

In the subchondral bone the blood vessels were increased in number 
and markedly congested. The marrow spaces were increased in size to 
such an extent that the bony trabecular were entirely gone in places and 
in other places were very much thinner than normal. The marrow spaces 
contained congested blood vessels, a large amount of fibrin, a few fibro- 
blasts and a few marrow cells with only here and there a giant cell. 

In the older calf the changes were identical with that of the younger 
one. In addition there was beginning erosions on the corresponding tibial 
articular surfaces. 

All the other joints of both calves were apparently normal. 

These are cases of acute fibrinous synovitis and acute erosive osteo- 
arthritis caused by B. coli infection, probably through the umbilical vein. 

Case n. — A heifer calf, two weeks old, received for diagnosis. She 
died of acute hemorrhagic enteritis. 

Both hock joints contained a reddish gelatinous substance. In the 
tibio-astragalar articulations there were reddened erosions 2.5x1 centi- 
meters on the tibial articular surfaces. The astragalar articular surfaces 
were normal. 



230 GOLDBERG. 

Microscopically, in the eroded area the cartilage was nearly gone. There 
remained a thin imperforated layer in which the matrix took a pinkish 
stain. There was some vascularization, in the center as well as at the 
periphery of the erosion, by engorged capillaries emanating from the sub- 
chondral bone. In the cartilage that was not affected by erosion the 
superficial half stained pinkish, while the half toward the epiphyseal bone 
took a bluish stain. 

In the subchondral bone the marrow spaces were enlarged and contained 
numerous engorged blood vessels, fat cells, fibroblasts, giant cells, various 
marrow cells, and some fibrin. They were larger in the center of the 
epiphysis than, they were towards the articular cartilage, but the latter 
contained most of the congested blood vessels and the giant cells. The 
greatest amount of destruction of bone, however, was in the diaphysis, 
just beneath the epiphyseal cartilage. Here there was a large amount of 
fibrin and a large number of endothelial cells in the marrow spaces in 
addition to structures similar to those found in the subchondral epiphyseal 
marrow spaces. Here also the marrow spaces coalesced, due to absorption 
of some of the bony trabecular. 

Of the other joints of the body, in the hip joints, in the posterior 
metatarso-phalangeal, and in the elbow joints the articular cartilages were 
*of a bluish color. In the stifle joints the synovial membranes were pink- 
ish and contained hemorrhages, the cartilages were bluish and the contents 
were gelatinous. The remaining joints were normal. 

This is a case of acute erosive osteoarthritis resulting from scours in 
which the causative agent was apparently in the joint as well as in the 
subchondral bone. 

Case 13. — A three-weeks-old heifer calf killed on account of scours. 
On autopsy there was found a fibrinous pleurisy and pneumonia as well as 
an acute catarrhal gastro-enteritis. 

In the hock joints all the bones showed extensive erosions with the car- 
tilages entirely gone in places. The joint cavities were filled with fibrin. 

Both scapulo-humeral and both humero-radial joints were filled with 
fibrin and there was edema around them. The humero-radial joints 
showed, in addition, small erosions in the humeral and the radial articular 
cartilages. The remaining joints were normal. 

Cultures showed a micrococcus albus, a streptococcus, and B. coli. 

This is a case of an acute erosive osteoarthritis and a fibrinous syno- 
vitis, apparently caused by umbilical infection. 

Case 16. — Left leg of a two-months-old colt received for diagnosis. 

In the stifle joint the capsular ligament was thickened in places. The 
synovia was turbid and contained flocculi. The synovial membrane was 
almost completely covered by yellowish filiform and flattened villous tufts, 
varying in length from 1 millimeter to r centimeter. In one place two 
parts of the synovial membrane were adherent by a smooth band of con- 
nective tissue 8 millimeters wide, 2 millimeters thick, and 7 centimeters 



THE PATHOLOGY OF SPAVIN. 23 I 

long, running across the median end of the patella and attached to the 
lower border of the patellar articular cartilage (Fig. 7). 

In the femoro-patellar articulation the femoral articular cartilage was 
thinner than normal nearly throughout. This area was studded with 
punctiform reddened erosions. The subchondral bone was reddened. 
The patellar articular surface was normal, excepting a small erosion near 
the superior border and a fibrous attachment at the inferior border. The 
external lateral ligament was macerated and appeared shreddy. 

In the femoro-tibial joint the cartilage on the center of the median ridge 
was gone for an area of 3.5 x 2.5 centimeters. The denuded bone was 
smooth and shiny and of a brownish gray color. The corresponding 
tibial articular surface was similarly affected for an area two centimeters in 
diameter. The cartilaginous disc was gone at this point, and at the periph- 
ery it was covered by villous tufts. On the lateral femoral trochlear ridge 
the articular cartilage was of a bluish color. There were punctiform 
erosions near the anterior and external border for an area of 2 x 1 
centimeters. The corresponding tibial articular surface and that of the 
cartilaginous disc were normal. 

In the hock joint the capsule was of normal thickness. The synovial 
membrane was covered nearly throughout by reddened fibrous tufts vary- 
ing in length from 1 to 1.5 centimeters. Most of these were filiform, but 
some were flattened. Between the small bones the synovial membrane 
was roughened by fine reddened tufts. 

In the tibio-astragalar articulation there was an area six millimeters 
square, in the center of the tibial trochlear ridge, slightly roughened by 
very shallow, punctiform depressions. There was a similar area on the 
median side of this ridge. 

Microscopically, the cartilage contained areas where the nuclei were 
visible, but did not take the nuclear stain. At the periphery of these 
areas there were nests containing numerous cells in which the nuclei 
stained deeply. These areas were near the subchondral bone. 

The subchondral marrow spaces were enlarged, and contained vessels 
engorged with blood and some fibroblasts. 

The corresponding astragalar articular surface was more markedly 
affected. There was a purple shallow erosion 1.5 centimeters x 6 milli- 
meters in the trochlear groove. On the median side the erosion was 
slightly deeper, otherwise it was similar to the one on the corresponding 
tibial articulation. 

Microscopically, in the deepest part of the erosion the cartilage was 
thinner than normal. In other places there were necrotic areas in the 
cartilage. Some of these areas extended from the subchondral bone to 
the surface of the cartilage. Others were situated near the subchondral 
bone and did not extend to the articular surface. At the periphery of 
these necrotic areas there were nests containing numerous deeply staining 
cartilage cells. 

In the subchondral bone the changes were similar to those of the tibial 
articulation, but they were more marked. 



232 GOLDBERG. 

The calcaneo-astragalar joint and the articulation between the astraga- 
lus and the central tarsus were bluish in places, otherwise apparently 
normal. 

The remaining joints of this leg were normal. 

Media inoculated from the joints gave a growth of B. coli. 

This is a case of a subacute proliferative sero-fibrinous synovitis and 
erosive osteoarthritis apparently caused by infection. 

Case 21. — A five-months-old bay colt that died of gangrenous pneu- 
monia, ten days after an operation on a large edematous growth in the 
scrotal sac. 

Both scapulo-humeral joints showed erosions one centimeter in diameter 
on the humeral and on the corresponding scapular articular surfaces. 
In the humero-radial joints there were large triangular- shaped erosions on 
the humeral and the radio-ulnar articular surfaces. In all the fetlock 
and the corono-pedal joints the synovial membranes were hemorrhagic 
and the articular cartilages showed small, rounded, reddened erosions. 
In the carpal joints the synovial membranes were hemorrhagic, otherwise 
the joints were normal. 

In the right hock joint the capsular ligament was normal in thickness. 
The synovial membrane of the tibio-tarsal articulation was almost entirely 
covered with yellowish white villous tufts, varying in length from i milli- 
meter to i centimeter. The synovial membranes of the intertarsal and 
tarso-metatarsal articulations were covered, in places, with short villous 
and flattened tufts. The interosseous ligaments were reddened by 
hyperemia. 

There was a shallow, bluish erosion 1.5 centimeters x 6 millimeters in 
the center of the tibial trochlear ridge. There was a similar erosion 
3 centimeters x 5 millimeters on the corresponding astragalar articular 
surface. 

In the calcaneo-astragalar articulation there was a bluish erosion 
2 centimeters x 2 millimeters x .5 millimeter in the angle of the lateral 
astragalar articular facet. There was a similar, but very shallow erosion 
on the corresponding calcanean articular facet. The remaining articular 
cartilages of the hock joint were of a bluish color, otherwise apparently 
normal. 

The left hock joint contained a little yellowish, turbid synovia with 
flocculi of fibrin. The capsule was of normal thickness. The synovial 
membrane of the tibio-astragalar articulation was covered over half its 
surface by villous tufts, varying in length from 1 millimeter to 1 centi- 
meter. In the center of the tibial trochlear ridge there was a slightly 
noticeable erosion 1.5 centimeters x 7 millimeters. The base of this 
erosion was covered by a thin layer of cartilage. On the corresponding 
astragalar articular surface there was a deeper bluish erosion 1.5 centi- 
meters x 4 millimeters x 1 millimeter. 

In the calcaneo-astragalar articulation there was a purple-colored erosion 
1 centimeter x 2 centimeters x .5 millimeter in the angle of the lateral 



THE PATHOLOGY OF SPAVIN. 233 

astragalar articular facet. The corresponding calcanean articular surface 
was similarly, but very slightly affected. There was a flattened transparent 
growth of connective tissue projecting from the synovial membrane into 
this eroded area. 

In the articulation between the astragalus and the central tarsus there 
was a flattened growth of connective tissue on the synovial membrane 
projecting into the joint cavity for a distance of one millimeter. There 
was a similar growth on the synovial membranes in the articulation 
between the central and the third tarsus, and in the tarso-metatarsal 
articulation. 

There was a fibrous ankylosis between the central and the third tarsus 
that emanated from the space around the interosseous ligament and that 
ran antero-posteriorly for a distance of 8 x 2 millimeters. The cartilage 
immediately surrounding the ankylosed area was depressed. 

The remaining articular cartilages of the hock joint were bluish, other- 
wise apparently normal. 

Microscopically, in the shallow erosions the cartilage was thinner than 
normal, and covered by cells resembling flattened endothelial cells. The 
cartilage immediately underneath resembled fibro-cartilage, and that 
nearer the bone appeared normal. At the periphery of the erosion the 
superficial layer of cartilage took a pinkish stain, while the deeper layers 
stained blue. 

In the subchondral bone some of the marrow spaces were enlarged and 
filled with numerous, very markedly congested blood vessels, some 
lymphoid marrow, and fat cells. Those farther away contained few con- 
gested blood vessels and fat cells. 

In the deeper erosions the microscopical changes were the same, except- 
ing more marked. 

This is a case of subacute proliferative synovitis and erosive osteo- 
arthritis, and an acute hemorrhagic synovitis and erosive osteoarthritis 
in some of the joints. In the articulation between the left central and 
third tarsus there was a chronic fibrous ankylosing osteoarthritis. 

Case 22. — A black pure-bred percheron colt, six months old, killed on 
account of gonitis. 

The left coxo-femoral articulation contained about a tablespoonful of 
clear yellow fluid. The cartilage of the cotyloid cavity was slightly 
roughened. 

The left stifle contained 340 cubic centimeters straw-yellow, slightly 
viscid fluid with yellowish white flocculi. The lateral femoral trochlear 
ridge was eroded for an area of 8 x 2.5 centimeters. At the rim of this 
erosion, near the attachment of the capsular ligament, the synovial mem- 
brane was gone for an area of 7 x 4 centimeters. The ligament under- 
neath was flabby and thready appearing, as if it were chewed, due probably 
to its being caught between the patella and the trochlear ridge as the 
former slipped out of its place. The rest of the capsule appeared slightly 
thickened. The synovial membrane was thickened by fibrous tufts, the 



234 GOLDBERG. 

larger of which were about five millimeters long. This was most pro- 
nounced at the insertion of the capsule and gradually disappeared away 
from that point. 

At the upper edge of the erosion there were several pieces of cartilage 
of apparently normal structure and barely attached to it by what seemed 
to be threads of softened cartilage. The erosion presented a central area 
4 x i centimeters where the cartilage was entirely gone and the denuded 
bone was reddened and rough. Around this area the cartilage appeared 
as if it had been chewed off and was becoming smooth, probably by the 
friction of the slipping out of the patella. 

The patella showed an erosion two centimeters in diameter on the 
surface corresponding to the erosion on the lateral femoral trochlear ridge. 
On the synovial membrane surrounding the patella there were fibrous tufts 
similar to those described above, except for an area five centimeters long 
at the external capsular attachment where the synovial membrane was 
normal. 

In the right stifle there were subcutaneous hemorrhages, ecchymoses, 
for an area of 6 x 4 centimeters. One hundred cubic centimeters of thick, 
turbid, reddish brown fluid was removed from the joint. The capsule was 
divided into pockets so that some pockets contained clear straw-yellow 
fluid, while others contained the above-mentioned cloudy fluid. The 
pockets were all tense and under pressure. The liquid was forced out, on 
incision, for a distance of about three feet. The cloudy fluid coagulated 
on standing. 

The capsule was thickened by connective tissue. There was edema 
around the capsule. The capsule contained ossified and chondrified areas, 
the largest one being 1 centimeter x 5 millimeters. The synovial mem- 
brane was thickened by fibrous tufts, some of which were threadlike 
while others were club-shaped or papilliform, most of them about 1.5 
centimeters long, projecting into the articular cavity. In the folds of the 
synovial membrane there were large flattened yellowish masses of coag- 
ulated fibrin that projected into the cavity. The edges of some of these 
were reddened. Some of these were free, while others were attached to 
the capsule. 

Microscopically, the masses lying free in the pockets of the synovial 
membrane were masses of granular, reticular, and homogeneous fibrin. 
On the surface of this fibrin were quite a few leucocytes and endothelial 
cells. In this area were seen a few cocci and rods. The masses attached 
to the synovial membrane were composed of connective tissue cells sur- 
rounding small blood vessels. Here and there were seen minute areas of 
cartilage and of bone (Fig. 9). This granulation tissue was covered by 
fibrin in which were seen some leucocytes. 

The medial femoral trochlea was of a bluish color and the cartilage was 
partly covered by masses of fibrin, otherwise it was apparently normal. 
The lateral trochlear ridge presented an erosion at its lower half 4 centi- 
meters x 2.5 centimeters x 1 millimeter. It was of a yellow color, lusterless, 
and studded with punctiform erosions. 



THE PATHOLOGY OF SPAVIN. 235 

Microscopic examination of the median femoral trochlear ridge showed 
that the articular cartilage was being dissolved in places by vascularization 
from the subchondral bone and by a marked fibrinous exudate. There 
were also a few giant cells and some endothelial cells. In the subchon- 
dral bone the marrow spaces were enlarged to such an extent that few 
bony trabecular remained. These spaces contained a marked fibrinous 
exudate and many congested capillaries. The marrow cells were more 
numerous nearer the articular cartilage than farther away (Fig. 2). 

The patella presented a small, deep, eroded area 1.5 centimeters x 8 
millimeters x 2 millimeters on the surface, which was applied to the ero- 
sion on the lateral femoral trochlear ridge. On the same side and a little 
lower there was a mass of organized fibrin attached to the cartilage as if a 
line were drawn across it. This seemed to come from the synovial 
membrane. 

Microscopically, the cartilage was apparently normal. This was covered 
by small blood vessels surrounded by connective tissue cells, /.^..granula- 
tion tissue. This granulation tissue varied in age, the oldest being next 
the articular cartilage and the youngest being covered by a thin film of 
fibrin about one-fourth the entire thickness of the band (Fig. 6). 

In the center of the patellar erosion the cartilage was gone. In place 
of the subchondral bone there were fibrous connective tissue cells sur- 
rounding congested blood vessels. On the surface of this tissue there was 
an exudate of fibrin containing bluish granules. The marrow spaces, 
beneath the granulation tissue, were enlarged and contained a consider- 
able amount of fibrinous exudate, congested blood vessels, marrow, and 
young connective tissue cells. Next to the bone they were lined by endo- 
thelial cells, a few giant cells, and a considerable number of osteoblasts. 
The cartilage on both sides of the erosion was markedly degenerated, that 
on one side dipping into the granulation tissue. Blood vessels were seen 
penetrating the neighboring cartilage. There were a considerable num- 
ber of giant cells subchondrally in this region. 

In the femoro-tibial joint the synovial membrane was thickened by red- 
dened fibrous tufts. There were fibrinous masses in the folds resembling 
those in the femoro-patellar joint. There was in addition a greenish yel- 
low mass of fibrin resembling a lump of fat. The cartilaginous pads 
appeared normal. 

In the right hock joint the capsule was normal in thickness, but the 
synovial membrane was thickened by filiform and a few papilliform fibrous 
tufts. In the tibio-tarsal articulation there was a roughened erosion 1 
centimeter x 5 millimeters x 1 millimeter on the median astragalar troch- 
lear ridge. On section the bone beneath the erosion was reddened for an 
area of two millimeters. Anterior to this erosion the cartilage had been 
worn off for an area of 1 centimeter x 6 millimeters wide. There were 
several punctiform erosions on the lateral trochlear ridge. There was also 
an erosion 4 centimeters x 4 millimeters x .5 millimeter in the trochlear 
ridge. 



236 GOLDBERG. 

Microscopically, in the center of the erosion on the median ridge, the 
cartilage was almost gone, but little connective tissue being in its place. 
On each side of this area the cartilage was replaced by connective 
tissue. There was also a replacement of bone by connective tissue. 
The fibrillae of the former were of a bluish tint while those of the latter 
were stained red. In the marrow spaces just beneath the articular carti- 
lage there were proliferating capillaries distended with blood with here 
and there a giant cell. There was also some fibrinous exudate. In the 
area where the cartilage had been replaced by connective tissue, some of 
the vessels projected into this tissue. Near' this area there were seen 
several nests of proliferating cartilage cells. The marrow spaces farther 
away were markedly enlarged at the expense of the bony trabecular. 
They were filled with fibroblasts, congested capillaries, and some fibrinous 
exudate. 

In the calcaneo-astragalar articulation there was a shallow erosion 8 x 
3 millimeters in the angle of the lateral astragalar articular facet. There 
was a similar but smaller erosion on the corresponding calcanean articular 
facet. 

In the articulation between the astragalus and the central tarsus there 
was a flattened growth of connective tissue on the synovial membrane 
projecting into the joint cavity for a distance of one millimeter. There 
was gelatinous material around this growth. 

The articulations between the central and third tarsus and between the 
third tarsus and metatarsus showed the same changes as those in the 
articulation between the astragalus and the central tarsus. On section of 
the hock, the third tarsus was markedly reddened for an area of three 
centimeters and throughout its thickness. There was a reddened area in 
the calcaneum forming a rim under its articular cartilage. 

All the other joints of the body were apparently normal. 

In cultures made from the joints a short streptococcus, staphylococcus 
albus, and Ps. pyocyaneus, were obtained. 

In this case, apparently, we have in the left stifle a marked serous and 
proliferative synovitis of long standing with a secondary erosive osteo- 
arthritis. 

In the right stifle there was apparently an acute sero-fibrinous synovitis 
which was being transformed into a chronic erosive osteoarthritis and 
proliferative synovitis. 

In the right hock joint there was an erosive osteoarthritis and prolifera- 
tive synovitis. 

The cause seems to have been an infection perhaps through the navel. 

Case 26. — A four-year-old Guernsey cow killed on account of lameness 
and general emaciation due to a chronic catarrhal enteritis. 

In the right hind leg the coxo-femoral joint was normal. In the stifle 
joint there were erosions on the distal end of the femur on the facets that 
are applied to the semi-lunar cartilages. The erosions were shallow and 
extended about two centimeters in diameter. The center of the semi-lunar 



THE PATHOLOGY OF SPAVIN. 237 

cartilages showed fibrillation. The corresponding articular surface of the 
tibia showed fibrillary degeneration. There was a normal amount of 
yellowish viscid synovia in the joint. The synovial membrane was thick- 
ened by grayish tufts. The femoro-patellar joint was apparently normal, 
excepting a small erosion about five millimeters in diameter on the lower 
border of the patella. Cultures taken from this joint remained sterile. 

In the hock joint the cartilages of all the bones were eroded in places, 
the remaining cartilage appeared reddened. 

The other joints were apparently normal, excepting the cartilages were 
reddened. 

In the left hind leg the coxo-femoral joint was apparently normal. 

In the femoro-patellar joint the synovial membrane was roughened and 
covered by punctiform hemorrhages. Reddened fibrinous masses were 
present in the joint. These were adherent to the synovial membrane. 
The articular cartilages were of a bluish color, and lusterless. There 
was a hemorrhagic area 2 centimeters x 4 millimeters on the femur, above 
and immediately posterior to the articular cartilage. 

In the femoro-tibial joint the capsule was thickened. The synovial 
membrane was of a brownish color, and it was thickened by papilliform 
tufts. The anterior surface of the external condyle of the femur was 
eroded for an area of 2 centimeters x 1.5 centimeters x 2 millimeters. 
This area was denuded of its articular cartilage. The denuded bone was 
smooth and shiny. Adjacent to and posterior to this area there was a 
similar eroded area from which the cartilage was not entirely worn away. 
On the internal side of the median condyle there was a shallow erosion 
about 1.5 centimeters x 5 millimeters x .5 millimeter. The semi-lunar 
cartilages showed fibrillation in places. The tibial articular cartilages 
were roughened and of a bluish color. 

Media inoculated from the femoro-patellar joint gave a growth of micro- 
coccus albus, aureus, and citreus. 

The hock joint showed erosions in all the articulations. 

The lower joints were apparently normal, excepting the cartilages were 
slightly reddened. 

In the fore legs the elbow joints showed erosions about 2.5 x 1 centi- 
meters on both the radio-ulnar and the humeral articulations. All the 
other joints were apparently normal. 

This is a case of a chronic erosive osteoarthritis and proliferative 
synovitis. There was also an acute fibrino-hemorrhagic synovitis of the 
left femoro-patellar articulation. The latter was evidently caused by a 
micrococcus infection. In the former the cause is unknown. 

Case 30. — An eight-year-old iron-gray percheron mare that died with 
fistulous withers that extended to the spinal cord. 

In both humero-radial joints there were erosions 2.5 centimeters long 
and 2 centimeters wide on the humeral articular surfaces. There were 
similar erosions on the corresponding radio-ulnar articulations, 



238 GOLDBERG. 

In the right hock there was a little yellowish clear synovia. The cap- 
sule was apparently normal. The synovial membrane was thickened by 
whitish villous tufts over about two-thirds of its surface. These varied 
from 1 millimeter to 2 centimeters in length. Some were filiform, while 
others were flattened. 

There was an irregularly shaped bluish erosion 1.5 centimeters x 5 
millimeters x 1 millimeter in the center of the tibial trochlear ridge. 
On the corresponding astragalar trochlear groove there was an erosion 
1 centimeter square and 1 millimeter deep on the anterior and lower 
border, and an erosion 5 x 2 x .5 millimeters near the posterior border. 
There was an erosion 1 centimeter x 6 millimeters x 1 millimeter on the 
median ridge of the astragalar trochlea. On the lateral ridge the 
cartilage was dull and softer than normal. 

In the calcaneo-astragalar articulation there was an erosion 1.5 centi- 
meters x 1 centimeter x .5 millimeter on the external astragalar articular 
facet. There was a similar erosion on the corresponding calcanean 
articular facet. In the base of this erosion there was a whitish growth of 
connective tissue. There was an erosion 1 centimeter x 5 millimeters 
x .5 millimeter on the median astragalar articular facet, and a similar 
erosion on the corresponding calcanean articular facet. 

In the articulation between the astragalus and the central tarsus the 
cartilage was roughened along the anterior border varying in width from 
3 to 6 millimeters. Near the median border and immediately behind the 
roughened surface there. was a whitish thickened roughened area 1 centi- 
meter x 5 millimeters x .5 millimeter at its thickest place. The corre- 
sponding articulation of the central tarsus was similarly affected. On 
drying the cartilage became dull yellow in color and extremely brittle, 
probably due to presence of lime salts in the cartilage. The astragalar 
and calcanean subchondral bones were reddened, varying in width from 
1 to 5 millimeters, the reddening being 1 millimeter away from the carti- 
lage. The periosteum near the upper and anterior articular margin of the 
central tarsus was thickened to about one millimeter. It was of a whitish 
color and soft in consistency. 

The articular surfaces between the central and the third tarsus were 
roughened. 

There was a fibrous ankylosis between the third tarsus and the meta- 
tarsus for an area of about 8x5 millimeters at the anterior border of the 
articulation, not involving the capsular ligament. There was a groove 
about 1 millimeter deep and .5 millimeter wide around the fibrous tissue. 
There was an erosion 1 centimeter x 5 millimeters x .5 millimeter on the 
third tarsus at the anterior border of the interosseous ligament. There 
was a similar erosion on the corresponding metatarsal articular surface. 
The subchondral bone was reddened in places. 

In the left hock joint the synovial membrane was not so extensively 
affected by fibrous tufts as that of the right hock joint. There was a 
similar erosion on the tibial trochlear ridge. On the corresponding 
astragalar articular surface the erosion in the trochlear groove was 3.5 



THE PATHOLOGY OF SPAVIN. 239 

centimeters x 1 centimeter x r millimeter. There was an erosion 8 milli- 
meters in diameter and 1 millimeter deep on the median astragalar 
trochlear ridge. There was an extensive roughening of. the cartilage 
around the latter erosion. 

In the astragalo-calcanean articulation the changes were similar to those 
of the right hock and similarly located. 

In the articulation between the astragalus and the central tarsus the 
synovial membrane on the median side of the articulation was thickened 
by a flattened growth of connective tissue, projecting into the joint cavity 
for a distance of two millimeters. The articular cartilages in this place 
were roughened by shallow erosions for a distance of 2 x 1 centimeters. 
The cartilage in this place was bluish. The remaining articular cartilage 
was apparently normal. 

In the articulations between the central and the third tarsus and between 
the third tarsus and the metatarsus the articular cartilages near the 
median border were roughened and bluish in color. The subchondral 
bones were reddened. 

The remaining joints of the body were apparently normal. 

Microscopically, in the center of the right tibial erosion the cartilage 
was nearly all gone, but the lowermost layer remained. Above that there 
were individual cartilage cells with a pinkish staining cell body and inter- 
cellular substance. This was covered by what appeared to be a mass of 
necrotic tissue in which the nuclei have disappeared. In this mass there 
were scattered fibroblasts. On the surface there was a thin layer of fibro- 
blasts and adult connective tissue cells. The zone of calcification has not 
been broken except in one point, at the periphery of the erosion, where it 
has been destroyed by subchondral congested blood vessels surrounded 
by fibroblasts. The cartilage in this place showed evidence of prolifera- 
tion. There were masses of bluish staining cartilage cells and there were 
nests containing numerous cells. The cartilage above this area was 
degenerated but intact. In the subchondral bone under the eroded area 
the marrow spaces were enlarged and filled with fat cells, congested blood 
vessels, and fibroblasts. Outside of this erosion the cartilage was nearly 
normal and the subchondral bone was somewhat denser than normal and 
slightly congested. A few of the subchondral Haversian canals were 
filled with congested blood vessels and fibroblasts. 

In the left tibial erosion the cartilage was nearly all gone, including the 
lowermost layer. There remained only a few cartilage cells in the center 
of the erosion. In the place of the cartilage there was a thin layer of 
fibroblasts and old connective tissue cells. At the periphery the bone 
projected nearly to the articular surface. The other changes were similar 
to those in the right tibia. 

The right astragalar erosion was more advanced than that of the right 
tibia. It was deeper, involving the bone more, and the connective tissue 
layer was narrower. The subchondral bone and the surrounding bone 
and cartilage were similar to those of the tibia. 



240 GOLDBERG. 

In the articulation between the central and the third tarsus there were 
subchondral foci of necrosis in the places that macroscopically appeared 
roughened. These foci involved in places the lowermost layers of the 
cartilage. In other places the foci of necrosis extended for a considerable 
distance into the bone. The cartilage covering these areas showed 
marked degeneration. The cartilage was broken only at one point where 
the bone was extensively involved. There was also degeneration of the 
cartilage near the synovial membrane. The subchondral bone, aside from 
the necrotic areas, was dense and the Haversian canals were only here 
and there enlarged and irregular in shape. All the Haversian canals 
were, however, filled with fibroblasts, adult connective tissue cells, and 
congested blood vessels. Some of the enlarged canals also contained 
fibrin and some lymphocytes and a few of them were filled with endothe- 
lial cells. 

In the articulation between the central tarsus and the astragalus the 
cartilage next to the synovial membrane was thickened and showed fibril- 
lary degeneration, that towards the center of the joint was thinner and 
degenerated. The subchondral bone was dense and congested. The 
neighboring synovial membrane was markedly congested and showed pro- 
liferation of mesothelial cells and blood vessels. The periosteum of the 
central tarsus was thickened by large cells resembling cartilage cells, lying 
in rows parallel with the fibers of the attached ligaments. These cells 
were lying singly, and in very few places they appeared in nests of two, 
probably due to multiplication. In several areas the periosteum of the 
third tarsus was similarly affected. The other parts were normal. 

This is a case of degenerative, erosive, and fibrous ankylosing osteo- 
arthritis and proliferative synovitis. Some of the changes, such as fibril- 
lary degeneration and the proliferation of the synovial membrane and of 
the periosteum, indicate a mild irritation. The other changes, including 
the fibrinous exudate, the hyperemia, and the necrosis in the subchondral 
bone indicate a severe irritation. They also indicate infection. It is pos- 
sible that this condition was caused by metastasis of microorganisms from 
the fistulous withers. This at first produced mild irritation, and with the 
lowering of the resistance of the animal, the microorganisms came to these 
joints in greater number and produced a severe irritation accompanied by 
the acute changes. 

The degeneration without any break in the continuity of the cartilages 
and the proliferation of the synovial membranes seem to indicate that the 
irritant was perhaps first in the joint. The necrotic foci and the other 
changes in the subchondral bone seem to indicate that there were, per- 
haps later, metastatic foci in the subchondral bone. 

Again, in the apparently unaffected parts of the articulations the sub- 
chondral bones were denser than usual. This perhaps indicates that this 
density of the bone, the erosions in the tibio-tarsal articulations, and the 
tufts on the synovial membranes are vestiges of a previous inflammation. 
It may also be that in this animal the bones were naturally denser than 
usual. In the latter case the conclusion that in this case the irritant was 



THE PATHOLOGY OF SPAVIN. 24I 

both in the subchondral bone and in the joint cavity, or perhaps that it 
was in the joint cavity first and later in the subchondral bone also, may be 
justified. In the former case, where the assumption is that the mild 
changes are due to a previous inflammation, it is possible that in both 
inflammations the origin was in the subchondral bone. 

Case 35. — A fifteen-year-old red roan gelding that died with a gangre- 
nous pneumonia. 

In each scapulo-humeral joint there was a triangular erosion on the 
humeral heads. The remaining cartilages were bluish. In the humero- 
radial joints there were erosions 4 centimeters x 2 centimeters x 3 milli- 
meters on the humeral, and on the corresponding radio-ulnar articular 
surfaces. The rest of the cartilage was bluish. In the carpal joints the 
synovia was reddish. The cartilages were bluish and eroded in places. 

In the stifle joints the synovial membranes were thickened and rough- 
ened by a reticular growth of connective tissue. 

On the outside, in front and above the left hock, there was a swelling 
3x2x2 centimeters, composed of edematous connective tissue. 

The joint cavity contained about a tablespoonful of yellow viscid synovia. 
There was a small pocket on the external side containing a mass of partly 
organized fibrin. 

The synovial membrane was thickened anteriorly by reddish villous 
tufts, about one centimeter long. Posteriorly the synovial membrane 
was similarly affected, except that the tufts were yellowish. The articu- 
lar cartilages of the tibio-astragalar joint were of a slightly bluish tinge 
in places. There was a very shallow erosion, 6 centimeters long and 
2 millimeters wide, in the astragalar groove. There were two punctiform 
erosions on the corresponding tibial trochlear ridge. On section there 
was marked subchondral hyperemia in all the bones of this joint. 

In the calcaneo-astragalar joint there was an erosion 2 centimeters x 
1 centimeter x 1 millimeter on the lateral astragalar and on the correspond- 
ing calcanean articular surfaces. This area was filled with a yellowish 
brown gelatinous mass. There was a smaller erosion on the median 
facets of these bones, partly filled with a similar mass. The remaining 
cartilages were bluish in places. There was a shallow erosion six milli- 
meters in diameter on the astragalus near the interosseous ligament, and 
a similar erosion on the corresponding articular surface of the central 
tarsus. The articular cartilages of the third tarsus and of the correspond- 
ing articular surface of the metatarsus were roughened in places. 

On the external surface of the right hock there was a fluctuating swell- 
ing 6x4x2 centimeters on the median side posterior to the tibia, just 
above the articulation. On opening, it showed that it was a dilatation of 
the articular capsule at that point. The contents were synovia, and a free 
irregular mass 2.5 centimeters x 2 centimeters x 3 millimeters, composed 
of shreds of fibrin mixed with synovia. There was also a partly organized 
mass of fibrin adherent to the synovial membrane. The synovial mem- 
brane was thickened by villous tufts that were anteriorly of a reddish color 



242 GOLDBERG. 

and posteriorly grayish. The dilated part also was lined by villous tufts. 
The tibial and astragalar articular cartilages were of a slightly bluish 
color, and contained grooves running from before backwards and parallel 
to each other. These grooves were i to 6 millimeters apart, each being 
i millimeter wide. 

On section of the hock, there was marked hyperemia subchondrally in 
all the bones. 

There were several shallow erosions in the calcaneo-astragalar articula- 
tion. The remaining cartilages were bluish in places, otherwise normal. 

Microscopically, in the erosion on the left astragalar trochlea the car- 
tilage was thinner than in the other parts of the articulation. The remain- 
ing cartilage in the eroded area, as well as the surrounding cartilage, 
showed fibrillary degeneration. The subchondral bone was normal (Fig. 
3). In the right tibio-tarsal articulation the grooves were of various 
depths, varying from places that showed a dent in the articular cartilage 
to those in which the cartilage has entirely disappeared, leaving the sub- 
chondral bone denuded of cartilage. The remaining articular cartilage 
showed fibrillary degeneration. The cartilage showed in many places 
nests filled with numerous cartilage cells in which the nuclei were very 
small. The subchondral bone showed slight congestion. 

In all the other joints of the body the cartilage was of a bluish color, 
otherwise apparently normal. 

This is evidently a case of subacute fibrinous synovitis and degenerative 
erosive arthritis. This originated apparently in the joints, since the sub- 
chondral bones are normal and there is no break in the continuity of the 
cartilage. 

Case 39. — An aged sorrel mare that died with a ruptured diaphragm. 

In the left scapulo-humeral joint there was a yellowish erosion 1 centi- 
meter in diameter and 1 millimeter deep on the scapular articular surface. 
There was a similar erosion on the corresponding humeral articular sur- 
face. In the humero-radial joint there was a large, yellowish erosion on 
the radio-ulnar articular surface and a similar erosion on the correspond- 
ing humeral articulation. On the latter articular surface there were also 
small, scattered erosions, varying in size from 2 millimeters to 1 centi- 
meter in diameter and .5 to 2 millimeters deep. In the fetlock joint 
there were small depressions one millimeter in diameter in the groove of 
the first phalanx. In the center of these depressions there were whitish, 
calcified points. The remaining articular cartilage was apparently normal. 

In the right hock joint the synovial membrane was thickened by villous 
tufts. There was a yellowish erosion 2 centimeters long, 1 centimeter 
wide, and 1 millimeter deep, in the center of the tibial trochlear ridge. 
There was a yellowish erosion 4 centimeters x 3 millimeters x .5 milli- 
meter in the astragalar trochlear groove. There was an erosion 1.5 cen- 
timeters x 1 centimeter x .5 millimeter on the internal face of the lateral 
trochlear ridge. Surrounding this there were several punctiform erosions 
and one white calcified point about .7 millimeter in diameter. 



THE PATHOLOGY OF SPAVIN. 243 

In the calcaneo-astragalar articulation there was a whitish and yellow- 
ish erosion 2 centimeters x 5 millimeters x .5 millimeter on the lateral 
astragalar articular surface. There was a yellowish erosion 5 millimeters 
square and .5 millimeter deep on the median astragalar articular surface. 
There were similar erosions on the corresponding calcanean articular sur- 
faces. The remaining articular surfaces were bluish in places, otherwise 
apparently normal. 

Microscopically, in the erosions the zone of cartilage next to the bone 
was the only cartilage left. The rest of the cartilage was gone. Its place 
was taken by a homogeneous pinkish staining substance containing con- 
nective tissue cells. At the periphery of the erosion the upper layers of 
cartilage cells were degenerated. In the subchondral bone the marrow 
spaces were enlarged and filled with fat cells and congested blood vessels. 

In the left tibio-astragalar articulation the synovial membrane and the 
tibial trochlea showed changes similar to those in the right hock joint. 
There was a yellowish erosion 3 centimeters x 1.2 centimeters x 1 milli- 
meter in the astragalar trochlear groove. There was an erosion six milli- 
meters in diameter in the middle of the median trochlear ridge. The 
subchondral bone of this articulation was reddened. 

In the calcaneo-astragalar articulation there was an erosion 8 x 5 x .5 
millimeters on the lateral calcanean articular facet and a similar erosion on 
the corresponding astragalar articular surface. The median articular 
facets were normal, except at the lower border for an area of 1 centi- 
meter x 5 millimeters where the cartilage was of a purple color. 

The articulation between the astragalus and the central tarsus was 
normal, excepting a few spots where the cartilage was of a purple color. 
These spots were irregularly distributed over the entire articular surface. 

In the articulation between the central and the third tarsus the anterior 
and median margins of the articular cartilages were eroded. The borders 
of the erosions were irregular. In some places there were depressions 
and in others there were elevations. The elevated areas in the erosions 
were due to a growth of whitish connective tissue. In places the two 
bones were grown together by connective tissue. In these places the 
synovial membrane was grown fast to the bones. This area was about 
eight millimeters wide. 

In the center of the third tarsus there was a yellowish, roughened, 
raised calcified area one millimeter in diameter. There was a depression 
on the corresponding articular surface of the central tarsus. There was a 
shallow, roughened erosion five millimeters in diameter in the posterior 
part of the third tarsus and a similar erosion on the corresponding articu- 
lar surface of the central tarsus. 

In the articulation between the third tarsus and the metatarsus the 
anterior border was roughened for a distance of about two millimeters in 
width. Otherwise the articular cartilages were normal. 

The hind fetlock joints were normal, except that the synovial membranes 
were covered with reddened villous tufts. In the left hind leg, in the 
articulation between the first and second phalanges, the two bones were 



244 GOLDBERG. 

grown together by partial osseous ankylosis. There was also a peri- 
articular paraostosis in the form of a smooth bony growth 1.5 centimeters 
thick and 5 centimeters long. Between the bones and the bony out- 
growth there was a thin layer of connective tissue. There was a ringbone 
in the right hind leg on the distal end of the first phalanx not involving 
the articulation. 

The right fore leg was not examined. 

The remaining joints were apparently normal. 

This is a case of a chronic erosive osteoarthritis and proliferative 
synovitis with a chronic fibrous ankylosing osteoarthritis of the left hock 
joint and a chronic osseous ankylosing osteoarthritis and periarthritis of 
the left phalangeal joint. The subchondral and subsynovial hyperemia 
was probably due to the cause that produced the death of the animal. 

Case 40. — An aged bay mare that was killed on account of chronic 
pulmonary emphysema. 

In both coxo-femoral joints the articular cartilages of both the cotyloid 
cavities and the corresponding femoral heads were thickened, wrinkled, 
and of the consistency of soft rubber. The synovial membranes were 
normal. 

In the left hock joint the synovia was normal. The capsular ligament 
was normal in thickness. The synovial membrane was thickened and 
roughened by a reticular growth of connective tissue. 

In the center of the tibial-trochlear ridge there was an erosion 1 centi- 
meter x 5 millimeters x .5 millimeter. In the base of this erosion there 
was a growth of whitish connective tissue. There was a similar erosion 
in the corresponding astragalar groove. There was considerable roughen- 
ing of the cartilage on the lateral articular surfaces of this joint. 

In the calcaneo-astragalar articulation there was an erosion 1 centimeter 
x 4 millimeters x 1 millimeter in the angle of the lateral astragalar 
articular facet. The base of this erosion was yellowish, containing reddish 
points in several places. There was a similar erosion on the correspond- 
ing calcanean articular facet. This erosion emanated from the space 
surrounding the interosseous ligament. 

The articulation between the astragalus and the central tarsus was 
normal. 

In the articulation between the central and the third tarsus there was 
slight roughening on the anterior and median margin of the articular 
cartilages. There was fibrous ankylosis near the posterior end of the 
interosseous ligament for an area of four millimeters in diameter. The 
synovial membrane of this articulation was normal. 

There was fibrous ankylosis between the central tarsus and the os 
tarsale I. et II. at the upper border, for a distance of two millimeters in 
diameter involving the synovial membrane. The cartilages around the 
ankylosed area were roughened by erosion. The remaining articular 
cartilages of the hock joint were normal. 



THE PATHOLOGY OF SPAVIN. 245 

In the right hock joint the tibio-astragalar articulation was similar to 
that of the left, except there was not so much connective tissue in the 
erosions. There were also a few reddened fibrous tufts on the synovial 
membrane in addition to the thickening of the latter by reticular 
connective tissue. 

The calcaneo-astragalar articulation was similar to that of the left hock, 
except the erosion contained a growth of whitish connective tissue. 

In the articulation between the central and the third tarsus there was 
fibrous ankylosis near the posterior end of the interosseous ligament for a 
distance of 5 x 2 millimeters running in an antero-posterior direction. 

There was fibrous ankylosis between the central tarsus and the os tarsale 
I. et II. similar to that of the left hock joint. 

The remaining articular cartilages of the hock joint were normal. 

The remaining joints of the hind limbs were normal. The fore limbs 
were not examined. 

Microscopically, in the ankylosed area the synovial membrane was 
obliterated. The bones were grown together by a homogeneous non- 
vascular mass containing degenerated cartilage cells and connective tissue 
cells. Some of each subchondral bone was replaced by that tissue. 
There was, however, a line of demarcation between the bone and this 
mass of tissue. This line stained blue, and was continuous on both 
sides of this mass, except at one point, where it was broken by an 
enlarged Haversian canal. This blue line was composed of cartilage 
cells, which in places showed evidence of proliferation. In the part of 
the joint that was not grown together the upper layers of the articular 
cartilages, on both surfaces, were necrotic. The layers next to the sub- 
chondral bones were degenerated. In the subchondral bones the Haver- 
sian canals were enlarged and irregular in shape. They were filled with 
fibrin, congested blood vessels, newly formed blood vessels, endothelial 
cells, fat cells, and fibroblasts. The periosteum in the vicinity of the 
ankylosed area was thickened by large cells lying in rows parallel with the 
fibers of the attached ligaments. 

This is a case of a chronic erosive and fibrous ankylosing osteoarthritis, 
and proliferative synovitis. 

Case 41. — The hock joints of an aged horse that died of swamp fever. 

In the right hock joint there was a bony outgrowth, 3x12x1 centi- 
meters, on the median side over the articulation between the upper and 
middle rows of tarsus. The astragalo-calcanean articulation was obliter- 
ated throughout its extent, excepting for a small area five millimeters long 
at the upper border. The obliterated part was reddened throughout its 
extent, the articular cartilages were apparently gone, and in places it 
seemed as if the two bones were grown together by fibrous tissue. In the 
articulation between the astragalus and the central tarsus there was an 
area one centimeter long immediately anterior to the interosseous liga- 
ment where the articular cartilages were gone and the bones were grown 
together by fibrous tissue. There was slight hyperemia around this area. 



246 GOLDBERG. 

The subchondral bone was reddened for an area extending from this liga- 
ment to the bony outgrowth on the median side. On the other side of 
the ligament the subchondral bone, as well as the articular cartilages, 
were apparently normal. There was a very shallow, uneven erosion 
12 x 5 millimeters in the astragalar trochlear groove, in the center of 
which there were whitish areas of connective tissue. There was no 
reddening of the subchondral bone in this eroded area. 

On the tibial trochlear ridge there was a whitish area, 3 centimeters x 
6 millimeters x 3 millimeters, that appeared as if an erosion was in this 
place and it had become healed, so that now the ridge was smooth 
throughout its extent. In the median trochlear groove there was a white 
growth of connective tissue on the articular cartilage 15 x 5 millimeters. 
There was a growth three centimeters thick on the median side of the 
tibia immediately above the articulation. It was composed of fibrous 
tissue and cartilage. 

Microscopically, in the periarticular bony outgrowth the marrow spaces in 
the central part of the newly formed bone were large and filled with con- 
gested blood vessels, fibrin, fibroblasts, and lined with fibroblasts and 
here and there a giant ceil. In place of the synovial membrane there was 
an area of cartilage cells arranged in rows perpendicular to the articular 
surfaces. Next to this area the two articular surfaces were grown together 
by cartilage and connective tissue cells. Toward the center of the articu- 
lation there was a considerable amount of a pinkish staining homogeneous 
substance, apparently the remains of the upper layers of the cartilage. 
The cartilage next to the subchondral bone was intact except near the 
edge of the articulation. The periosteum on each bone under the newly 
formed bone was intact. In the subchondral bone at the articular border 
the Haversian canals were enlarged and filled with fibroblasts and con- 
gested blood vessels. Toward the center of the articulation the Haver- 
sian canals were enlarged and filled with congested blood vessels and fat 
cells. On the outside the newly formed bone was covered by a large 
amount of connective tissue. 

In the calcaneo-astragalar articulation, at the proximal border, the upper 
layers of the cartilage were pinkish and homogeneous, and the two articu- 
lar cartilages were separated by the joint space. Approaching toward the 
center of the articulation the cartilages were the same, but the joint space 
was filled with connective tissue cells and fibroblasts. Farther down the 
necrotic parts of the cartilage were gone. In their place was a mass of 
connective tissue cells and fibroblasts containing numerous congested 
blood vessels running in various directions. On each side of this mass 
were several bony lamellae lined by osteoblasts and attached to the lower 
layers of cartilage. The joint space was of course obliterated (Fig. 8). 
Still farther down there was complete osseous ankylosis, with here and 
there a few cartilage cells remaining. In this part the marrow spaces were 
filled with fibroblasts and congested blood vessels. In the rest of the 
joint there was complete osseous ankylosis. In this part the bone was 
somewhat denser than the surrounding bone, and the marrow spaces 



THE PATHOLOGY OF SPAVIN. 247 

were filled with fibroblasts, congested blood vessels, fibrin, and fat 
cells. In the surrounding bone the marrow spaces were filled with fat 
cells and a few congested blood vessels. The neighboring periosteum 
showed slight proliferation. 

In the articulation, between the astragalus and the central tarsus near 
the interosseous ligament, there was a small area of osseous ankylosis in 
which the bone was denser than the surrounding bone, and the Haversian 
canals were filled with fibroblasts. Around this area the articular car- 
tilages were nearly normal, and the surrounding bone was slightly 
congested. There was also a small area of fibrous ankylosis in which the 
fibrous tissue contained numerous fibroblasts and congested blood vessels 
of various sizes. Next to the bone there were areas of cartilage. 
Around this ankylosed area the upper layers of the cartilages have gone, 
and the layers next to the bones were covered by granulation tissue 
similar to that in the ankylosed area. This tissue was being transformed 
into bone. This was shown by the presence of bony lamellae applied to 
the remaining cartilage and lined by osteoblasts. In the subchondral 
bones the Haversian canals were enlarged and irregular in shape. They 
were filled with fibroblasts, fibrin, and congested blood vessels (Fig. 11). 

In the white-colored area in the center of the tibial trochlear ridge the 
cartilage was entirely gone. Its place was taken by connective tissue 
containing some cartilage cells. The usual zones of articular cartilage 
were absent. At the periphery there were nests of proliferated cartilage 
cells. In the surrounding cartilage the upper layers showed degeneration. 
In the subchondral bone some of the Haversian canals were enlarged, 
irregular in shape, and contained congested blood vessels and fibroblasts. 

In the left hock the capsular ligament was slightly thickened. The 
synovial membrane was smooth, excepting along the margins where the 
various bones were in apposition. Along these margins the synovial 
membrane was thickened by whitish fibrous tufts varying in length from 
1 millimeter to 1 centimeter, the longest being in the tibio-astragalar 
articulation. 

There was a yellowish erosion 1.5 centimeters x 6 millimeters x 1 milli- 
meter in the center of the tibial trochlear ridge. There was a similar 
erosion 3 centimeters x 5 millimeters x 1 millimeter on the corresponding 
astragalar articular surface. The remaining articular cartilages were 
roughened in places and softer than normal. They had a sort of velvety 
appearance. 

In the calcaneo-astragalar articulation there was an erosion 1 centi- 
meter x 8 millimeters x 1 millimeter on the lateral astragalar articular 
facet. At the lower border of this erosion there was a growth of connec- 
tive tissue. There was a partly reddish and partly yellowish erosion 
6 x 2 x .5 millimeters on the median astragalar articular facet. There 
were similar erosions on the corresponding calcanean articular facets. 

The articulation between the astragalus and the central tarsus was 
apparently normal. 



248 GOLDBERG. 

In the articulation between the central tarsus and the third tarsus there 
was complete osseous ankylosis at the lateral and anterior aspects of the 
articulation, not involving the capsular ligament or the synovial mem- 
brane. In the ankylosed part the bone was denser than the porous bone 
of that part, but not as dense as the cortical bone. The ankylosed area 
was somewhat reddened. Near the middle of the articulation the bones 
were partially ankylosed, some of the cartilage remaining intact. The 
median margin was normal, but the cartilages near the median margin were 
roughened by shallow erosions. 

The remaining articulations of the hock joint were apparently normal. 

The lining of the calcanean bursa was slightly roughened throughout. 
On the lateral side of the tuber calcis for an area of 3x2 centimeters 
there were erosions surrounded by an excessive growth of connective 
tissue. 

This is a case of a chronic erosive, fibrous, and osseous ankylosing 
osteoarthritis and proliferative synovitis, as well as chronic ossifying 
periarthritis. 

Case 42. — An aged gray mare suffering from spavin of both hock 
joints. Killed by chloroform. 

In the left coxo-femoral joint the articular cartilages of both the coty- 
loid cavity and the head of the femur were thickened, wrinkled, and of 
the consistency of soft rubber. On section they showed fibrillation of the 
cartilage. The subchondral bone was apparently normal. 

In both stifle joints and. in the left carpal joint there were old yellowish 
erosions of the articular surfaces. 

In both hock joints in the articulations between the astragalus and the 
central tarsus the articular cartilages were entirely gone from both articular 
surfaces. The denuded bone was yellowish, smooth, and denser than 
normal, except in a small area where the denuded bone was roughened 
and reddened. In the right hock joint there was in addition fibrous 
ankylosis in several areas in the articulation between the central and third 
tarsus. 

Microscopically, the surface of the denuded bone was denser than 
normal. Towards the center of the bone the Haversian canals were 
enlarged, irregular in shape, and filled with granulation tissue. 

All the other joints were apparently normal. 

This is a case of a chronic degenerative arthritis and a chronic erosive 
and fibrous ankylosing osteoarthritis. 

Case 43. — A twenty-five-year-old buckskin mare extremely lame on 
left hind limb. Killed by chloroform. There were fibrous tufts and 
adhesions on the pleura and the peritoneum. 

In the left coxo-femoral joint there were yellowish erosions 1.5 centi- 
meters in diameter on the corresponding articular surfaces. Both stifle 
joints showed slight erosions. 



THE PATHOLOGY OF SPAVIN. 249 

Both hock joints were enlarged. The left was hard, while the right 
was fluctuating. There was osseous ankylosis between the two lower rows 
of tarsus and the metatarsus in both hock joints. In the left tibio- 
astragalar articulation there was a considerable amount of reddened 
synovia containing flocculi of fibrin. The synovial membrane was red- 
dened, roughened, and thickened by a partly organized fibrino-hemor- 
rhagic exudate. There was a reddish erosion 3x1 centimeters in the 
astragalar trochlear groove. There was a reddened triangular-shaped 
erosion on the median and an erosion 1 centimeter x 4 millimeters on the 
lateral astragalar trochlear ridge. There were corresponding erosions on 
the tibial articulation. In the right tibio-astragalar articulation the capsule 
was distended by a yellowish turbid liquid that coagulated on standing. 
A smear showed it to contain numerous polymorphonuclear leucocytes. 

Media inoculated from the left hock joint gave a growth of staphylo- 
coccus albus in pure culture. From the right hock joint there was a pure 
culture of B. coli producing gas in dextrose, lactose, and saccharose. 

This is a case of a chronic erosive and osseous ankylosing osteoarth- 
ritis apparently inactive at this time. There is also an acute fibrino- 
hemorrhagic synovitis and erosive osteoarthritis in the left hock joint, 
and a sero-purulent synovitis of the right hock joint. 

The cause of the long-standing condition cannot be determined at this 
time The acute conditions were apparently caused by infection. 

DISCUSSION. 

At the present time the term spavin stands for a chronic 
ankylosing intertarsal and tarsometatarsal osteoarthritis, 
with or without a chronic periarticular ossifying periostitis. 
It is supposed to originate in the subchondral bone as a rare- 
fying ostitis, and to spread to the articular cartilage, pro- 
ducing erosions and ankylosis, and to the periosteum, 
producing exostoses. 

In the sixty-five cases studied the pathological changes 
varied considerably. In the capsular ligament the early 
changes found were infiltration of polymorphonuclear leuco- 
cytes in two cases. In others, the capsular ligaments were 
thickened by a serous exudate and hemorrhage, while some 
showed round cell infiltration. In those of longer standing 
the most marked change was a thickening of the capsule by 
a production of connective tissue. In addition, there were in 
this connective tissue areas of cartilage and of bone. This is 
seen in the stifle joint, Case 22. In one case the capsular 
ligament was entirely ossified (left hind ring bone, Case 39), 



25O GOLDBERG. 

and in two instances one side of the capsular ligament was 
ossified (left stifle, Case 16, and right hock joint, Case 41). 

In the synovial membrane the early changes were hypere- 
mia and exudation. In some instances there were, in addi- 
tion, petechial hemorrhages on the synovial membrane. 
The exudate was purulent, sero-purulent, and fibrino-puru- 
lent, respectively. 

In many instances the exudate was mostly fibrin, and in 
still others there was a serous exudate. In two cases there 
was a sero-hemorrhagic and a sero-fibrino-hemorrhagic exu- 
date. The fibrinous exudate was in some cases free, while in 
others it was firmly adherent to the synovial membrane. In 
those instances where the fibrin was adherent it was brought 
about by an organization of the fibrin by connective tissue 
and blood vessels, arising from the synovial membrane. In 
one case there were areas of cartilage and of bone in this 
granulation tissue (Fig. 9). Many of these were in the form 
of small, round bodies attached to the synovial membrane by 
a small, villous outgrowth. This suggests a possibility of 
one of the ways in which free bodies may occur in a joint. 
Such a free body was found in one case to be composed of 
cartilage, the center of which had begun to ossify. 

Of the degenerative changes observed in the synovial 
membrane nearly all were of the nature of cloudy swelling 
of the lining mesothelial cells. This was rarely observed. 
As a rule the changes were proliferative instead. Necrosis 
of the synovial membrane was not found in these low-grade 
forms of arthritis. 

The proliferative changes of the synovial membrane were 
usually in the form of villous tufts varying in length from .05 
to two centimeters. These tufts were composed of various 
sized blood vessels surrounded by young and old connective 
tissue cells and covered by mesothelium (Fig. 7). Their 
appearance varied with the age of the process. In the early 
stages these tufts were small and reddened. In later stages 
they were longer and of a brownish color. In long standing 
cases they were whitish in color and composed mostly of 
adult connective tissue with a few blood vessels, and covered 



THE PATHOLOGY OF SPAVIN. 25I 

by mesothelial cells. Occasionally they were found inactive, 
i.e., they were the remains of a former inflammation. In 
these there were no fibroblasts. In many of the cases 
the proliferation of tissue was in the form of a connective 
tissue network on the synovial membrane. In several 
instances there were masses of connective tissue forming 
adhesions of different parts of the synovial membrane. In 
three cases of short duration there were outgrowths of blood 
vessels from the synovial membrane forming thin reddened 
arborous films on the edges of the articular surface (Fig. 7). 
Where the articular surfaces were ankylosed, the synovial 
membrane as well as the capsular ligament were, as a rule, 
replaced by bone. In one case the capsular ligament was 
ossified while the synovial membrane was represented by a 
line resembling cartilage. In another the synovial mem- 
brane was apparently not affected, although there was 
osseous ankylosis of the adjacent joint. 

While the changes of the synovial membrane were mainly 
exudative and proliferative, the changes of the articular 
cartilage were mostly degenerative. The appearance of the 
degeneration varied. In the early stages it manifested itself 
in a changed staining reaction. In this case the intercellular 
hyaline substance stained pinkish, while the nuclei gradually 
became smaller until they were represented by small gran- 
ules of nuclear material, which later disappeared, leaving a 
homogeneous pinkish staining matrix. This process was 
seen, in many instances, on the articular surface while the 
remaining cartilage was apparently normal. In other cases 
it took place around blood vessels that budded into the 
articular cartilage from the subchondral bone. By this 
process the cartilage became vascularized (Figs. 1 and 2). 
In some of the cases two processes were present simultane- 
ously, i.e., there was superficial degeneration of the cartilage, 
and at the same time vascularization from the subchondral 
bone. 

In many of the long standing cases the cartilage was 
thickened and softened. In some of these the consistency 
was that of soft rubber while in others, farther advanced, the 



252 GOLDBERG. 

cartilage was soft and fibrillated. Microscopically, the carti- 
lage was arranged in fibrils perpendicular to the articular 
surface (Fig. 3). In the cells near the surface the nuclei 
were nearly gone. They became larger as they approached 
the bone, and near the zone of calcification they appeared 
nearly normal. This process was produced experimentally 
by Cresswell in 1895 by means of long maceration and with 
the aid of pressure. He claims that chemically these fibrils 
are similar to connective tissue fibers. 

Necrosis of the articular cartilage appeared in the form of 
diffuse superficial necrosis and as circumscribed areas within 
the articular cartilage. This was manifested by a disappear- 
ance of the nuclei and a pinkish staining matrix. It was 
seen in the early stages in which there was a reaction to a 
more severe irritation. Superficial necrosis in the form of 
crateriform erosions was more common. In these the carti- 
lage had disappeared. In some of the cases the remains of 
the cartilage were in the form of a gelatinous mass. In 
others part of the cartilage was gone and the remainder was 
pinkish and homogeneous. In still others the cartilage was 
entirely gone, having been apparently liquefied and absorbed. 
Due to the fact that articular cartilage does not regenerate 
very readily, it is possible that some of these are the remains 
of a previous inflammation. 

In some of the erosions the articular cartilage was partly 
replaced by loose vascular connective tissue. In others the 
replacement was partly by dense non-vascular connective 
tissue. In a few the cartilage was entirely replaced by what 
appeared to be fibro-cartilage. In the cases where there was 
ankylosis of the articular surfaces the cartilage was replaced 
by loose vascular connective tissue, by dense non-vascular 
connective tissue, by porous bone, and by dense bone, 
respectively. In one instance where the cartilage was 
replaced by loose vascular connective tissue there was forma- 
tion of bone and proliferation of cartilage in this tissue 
(Fig. n). In another, where the cartilage was replaced by 
dense non-vascular connective tissue, there were areas of 
proliferating cartilage cells in this tissue. 



THE PATHOLOGY OF SPAVIN. 253 

The erosions in the center of the tibial trochlear ridge are 
designated by certain anatomists as synovial fossae. This 
would indicate that they consider them normal structures. 
In order to determine this point, a study was made of the 
joints of animals in utero as well as of older animals. In 
the cases designated as normal, the tibial trochlear ridges 
were found smooth and without a depression in the center. 
Some were found where the only variations from the normal 
were punctiform depressions on the ridge. A microscopic 
study of these so-called "synovial fossae" showed that they 
are undoubtedly pathological erosions. Some of them show 
a reaction to severe irritation, while others show reaction to 
mild irritants. There were found several in which it appeared 
that there was an erosion that had healed. In these healed 
erosions the zone of provisional calcification was absent and 
the cartilage resembled fibro-cartilage instead of hyaline 
cartilage. 

In some cases there were circumscribed areas of necrosis 
in the center of the articular cartilage. In a few of these 
the necrotic tissue was a homogeneous structureless mass. 
In most of them the necrotic areas were calcified. After 
decalcification these areas showed a homogeneous hyaline 
substance with numerous rounded bodies resembling " cor- 
pora amylacae " (Fig. 4). These areas are designated by 
Eberlein as " lime points." According to him they are 
areas in which the cartilage has been invaded by subchondral 
marrow, and which later had undergone a condensing 
process, i.e., they are areas of ossification in which the 
process had become quiescent in the stage of condensing 
ostitis. They show in effect one of the sequela? of necrosis. 
This is similar to necrosis in other tissues, particularly case- 
ation necrosis, which often becomes calcified. They do not 
contain any bone. 

In the subchondral bone enlargement of the marrow 
spaces by hyperemia and fibrinous exudate was the most 
marked feature in the early stages. A fibrinous exudate 
with numerous fibroblasts and congested blood vessels was 
found in the enlarged Haversian canals in some cases of long 



254 GOLDBERG. 

standing, even in those that showed fibrous ankylosis (Fig. 
10). In two cases there were polymorphonuclear leucocytes 
in addition to the fibrin. Some of the enlarged Haversian 
canals were completely filled with endothelial cells, and some 
were completely filled with fibroblasts. In many cases 
these canals were filled with fibroblasts, congested blood 
vessels, fibrin, and lined by osteoblasts (Fig. n). In some 
apparently quiescent cases, or those that have reached the 
last stages, particularly where there was osseous ankylosis, 
these canals were filled with fatty marrow with slight hyper- 
emia in certain instances (Fig. 8). 

In some cases where the articular cartilage was eroded, 
the subchondral bone was normal. This was true in those 
that showed fibrillation of the articular cartilage, as well as 
those in which there was no fibrillation (Figs. 3 and 5). In 
some cases in which the erosion did not reach the subchon- 
dral bone, the latter was denser than usual. While it is 
possible that this was due to a condensing ostitis, this con- 
dition was not confined to the affected area, so that it is 
more probable that the bone was naturally denser in these 
animals. In many of the cases the erosin affected the sub- 
chondral bone, as well as the cartilage. In these instances 
part of the underlying bone was gone and its place was 
taken by granulation tissue, and in one case by granulation 
tissue in which these were circumscribed areas of poly- 
morphonuclear leucocytes. 

In one instance there were foci of necrosis in the subchon- 
dral bone. These apparently began immediately under the 
cartilage and spread towards the center. The overlying car- 
tilage was degenerated, but intact. 

Eburnation of the denuded articular ends of bones was seen 
in two instances: in the left stifle joint (Case 16) and in 
both intertarsal articulations (Case 42). Eburnation is 
described as occurring in freely movable joints. In the lat- 
ter case the articulations between the central tarsus and the 
astragalus were affected. This joint is nearly devoid of 
motion. 



THE PATHOLOGY OF SPAVIN. 255 

In most of the cases there were no apparent changes in 
the periosteum. In some of them the periosteum was slightly 
thickened by a proliferation of large, bluish staining cells 
arranged in rows parallel to the fibers of the attached liga- 
ments. In one the periosteum was greatly thickened by 
connective tissue, and in three there was an ossifying 
periostitis. 

To summarize the changes, the final stage of the process 
is an osseous ankylosis of two adjacent bones. This process 
may be confined to the joint, or it may be accompanied by 
a periarticular ossification. This is, in many cases at least, 
preceded by a fibrous ankylosis. The fibrous tissue may be 
dense, non-vascular, with or without areas of proliferating 
cartilage. It may also be loose, rich in fibroblasts, and richly 
supplied with blood vessels (Figs. 8 and 11). In one case 
there was beginning ossification in this tissue. This form of 
ankylosis in some instances apparently began in the joint by 
an organizing exudate. The proliferation of tissue appar- 
ently began in the synovial membrane or around the inter- 
osseous ligament. In most cases it was impossible to tell 
where this form of ankylosis began. Preceding this stage 
there is erosion of the articular cartilage, with or without 
involvement of the subchondral bone. These erosions began 
in the subchondral bone in some cases. In others it undoubt- 
edly began in the joint sinus. In those that involved the 
bone, as well as the entire depth of the articular cartilage, it 
was impossible to determine the point of origin. The pro- 
liferation of the synovial membrane may start at any period 
of the process. The formation of villous tufts on the syno- 
vial membrane is so common that they have been considered 
as normally occurring " synovial villi." In this study nor- 
mal synovial membranes have been encountered in which the 
surface was whitish, smooth, and shiny, similar to that of 
other serous membranes. The early changes are hyperemia 
and exudation on the synovial membrane, hyperemia and 
exudation in the marrow spaces with widening of these, and 
degeneration of the articular cartilage. These changes may 






256 GOLDBERG. 

take place at the same time or they may occur individually. 
The process may become quiescent at various stages. 

The synovial membrane is the only structure in the 
immediate proximity of the joint sinus that is supplied with 
blood vessels. This makes the synovial membrane more 
resistant to irritation than the non-vascular articular cartilage. 
Regeneration of the articular cartilage does not take place 
very readily while all the structures of the synovial mem- 
brane regenerate with ease. For these reasons the same 
causative agent that would stimulate the synovial membrane 
to proliferation might produce degeneration and necrosis of 
the articular cartilage. The transition between the synovial 
membrane and the articular cartilage is gradual, so that 
there are blood vessels at the edge. This may account for 
the occurrence of the erosions a few millimeters from the 
articular border. Around the extreme articular border some 
of the cases studied show proliferative changes similar to 
those found on the synovial membrane. 

Practically nothing new can be advanced regarding the 
point of origin of spavin, since it has been ascribed to 
nearly every structure encountered in the neighborhood of 
the hock joint. It was thought to arise from the ligaments, 
bursas, tendons, and the synovial membrane around the hock 
joint. It was even thought that it originated from a gonitis. 
Finally, it was believed to originate from the articular 
cartilage and from the subchondral bone. Since Have- 
mann's discovery of the erosions in the joint, the specula- 
tions centered around the question whether the development 
of spavin was from within outwards, or from the outside 
inwardly. Beginning with Gotti and affirmed by most 
veterinarians of to-day, the former view was considered the 
correct one. 

In these cases, with three exceptions, all the bursae were 
apparently normal. In those that showed pathological 
changes, they were not of longer standing than the changes 
in the joint. It is undoubtedly possible that a traumatic 
injury of any kind may produce an ossifying periostitis 



THE PATHOLOGY OF SPAVIN. 257 

which may later spread to the synovial membrane and then 
to the joint. There is in this laboratory a dry specimen of 
a case of an ossifying periostitis not involving the joint. 
The coronary ring bone of the right fore leg in Case 37 and 
that of the right hind leg in Case 30 also illustrate this 
point. There are, however, numerous cases of spavin in 
which the periosteum is not involved, and, when involved, 
show changes that are less marked than those in the other 
structures of the joint. This is illustrated in many of the 
cases described in this paper, which shows conclusively that 
certainly not all cases of spavin originate in the periosteum. 
In many there were degeneration and erosions of the 
articular cartilage together with proliferation of the synovial 
membrane, without any affection of the bone. In these 
the zone of calcification was intact. In some the erosions 
began by a fibrinous exudate in the joint sinus. In these 
instances the point of origin was undoubtedly in the joint 
and not in the subchondral bone. In some of the cases the 
erosions began by vascularization of the articular cartilage. 
These blood vessels came from the subchondral bone. 
This makes it possible that in some instances the point of 
origin is in the subchondral bone. In one case there were 
necrotic foci in the subchondral bone while the articular 
cartilage showed degeneration. It seems that here the 
origin was in the subchondral bone. 

The erosions in these cases are on opposing articular 
cartilages. This is explained more readily on the assump- 
tion of an intra-articular irritation than as a subchondral 
irritation. Nathan holds that these are due to subchondral 
infective foci. This would mean that the foci were by 
chance in corresponding areas of the opposing bones. The 
cases where the erosions are exactly opposite each other are 
too numerous to be due to chance. It is possible that an 
irritant on the surface of the articular cartilage may be 
sufficiently severe to call forth a vascularization of the carti- 
lage from the subchondral bone. If this is so, it is possible 
that many erosions that appear to begin in the subchondral 
bone are in reality caused by an intra-articular severe irritant. 



258 GOLDBERG. 

Such an irritant on the cornea, particularly a bacterial irri- 
tant, will produce vascularization of the cornea. The carti- 
lage is likewise a non-vascular tissue, and it may react to a 
severe irritant in the same manner as the cornea. The 
erosions around the interosseous ligaments seem to indicate 
that the irritant producing them is in the joint proper. 

Since there are various forms of inflammations in the hock 
joint that may eventually lead to ankylosis and exostosis, 
it seems advisable to have the term spavin indicate any 
inflammation of the hock joint that may lead to ankylosis 
and exostosis. The meaning of the term spavin has been 
previously changed. As it stands to-day it does not include 
severe irritation in the joint which later terminates in anky- 
losis and exostosis. 

That the erosive forms of arthritis in the hock joint are 
included in the term spavin is evidenced by the various 
descriptions of this condition, beginning with Havemann's 
finding of these erosions. It seems advisable to include the 
exudative forms of arthritis in the hock joint, since they too 
may lead, and often do lead, to ankylosis and exostosis. 

The present views concerning the etiology of spavin are 
not entirely satisfactory. With few exceptions, mechanical 
irritation is considered as being the cause. It is thought to 
be brought about by pressure on the articular ends, stretching 
of tendons and ligaments. The erosions are described as being 
punctiform in the early stages. It seems doubtful that pres- 
sure in a joint should be concentrated in an area a millimeter 
in diameter. In those cases in which there was fibrillation 
of the articular cartilage, there is experimental data to show 
that it might be produced by pressure. Even here, how- 
ever, pressure alone does not seem to be sufficient to 
produce such changes. Traumatism is a satisfactory explana- 
tion only in those cases that apparently began with a perios- 
titis or an open joint. 

Considering the frequency of arthritis following diseases 
of other organs, — notably acute pneumonia, pericarditis, 
pleuritis, peritonitis, metritis, an ulcerated tooth, or other 
suppurating foci, — it seems possible that the true cause of 



THE PATHOLOGY OF SPAVIN. 259 

many a lameness is overlooked. The history is often unsat- 
isfactory. The lameness is often ascribed to a sprain where 
it may rather be a sequel of a forgotten inflammatory con- 
dition. Organisms may get into the circulation and finally 
lodge in the joints without producing any local lesion else- 
where in the body. The joints, not being richly supplied 
with blood, are favorable seats for multiplication of micro- 
organisms. 

Spavin is more common in some localities than in others. 
Here in Ithaca it is a common affection of horses. This has 
been ascribed to the hilly country. Dr. W. L. Williams 
claims that during his practice in the foothills of the Rocky 
Mountains spavin was rarely encountered. Certainly the 
Ithaca hills, then, cannot be the cause of the frequency of 
spavin. 

Various authors claim that spavin is more common in 
young than in older animals. Spavin is said to be most 
common in horses between the ages of two and four years. 
The reason for this fact, advanced by many authors, is the 
nervous temperament of younger horses. It is because 
" they attempt their work more vigorously than older ani- 
mals." This explanation does not seem to be very satis- 
factory. It seems possible that the reason spavin is less 
common in older animals is because of age immunity. 
Younger animals generally are more susceptible to infection 
than older ones. The nervous temperament may be a con- 
tributing factor. 

Many of these cases were undoubtedly caused by intra- 
uterine or umbilical infection. The variation of the lesions 
was apparently due to the variation of the resistance of the 
animals, the variation of the virulence of the cause, perhaps, 
and the variation in the ages of the processes. Case 22 is a 
notable example of well-advanced lesions caused by umbili- 
cal infection. A case similar to this one has been observed. 
It was about the same age, with a similar clinical history. A 
veterinarian ordered the destruction of the animal and the 
order was not followed. The animal recovered sufficiently 
to give eight years of valuable service. The dry specimen 



260 GOLDBERG. 

showed erosions in the right stifle and a spavin with articular 
and periarticular ankylosis of the left hock joint. 

In both these cases the cause was apparently local infec- 
tion resulting from umbilical infection. They show that it is 
possible for spavin to develop from umbilical infection. 

Schofield in his study of joint ill in foals concludes that it 
is closely associated with a hemolytic streptococcus, in which 
case the infection is probably by ingestion, since these organ- 
isms were found in the milk of the dam. Other means of 
infection are, according to him, intra-uterine and through the 
unhealed navel. He illustrates cases that recovered and 
those that resulted in ankylosis. 

Dr. W. L. Williams cites a case of a herd in which there 
were about fifty suckling foals. Many of the foals suffered 
from spavin, ring bone, and allied diseases. This herd was 
pasturing in a swamp. When the pasture was changed to 
dry land spavin ceased to exist in the herd. This case 
apparently corresponds to Saunier's " l'eparvin gras." 

In these foals running about freely in a pasture the cause 
does not seem to be in stretching of tendons, overexertion, 
heavy loads, or even excessive pressure on the cartilages. 
On the moist pasture infection seems to be the more likely 
cause of the spavins. The fact that it disappeared from the 
herd after change of pasture would strengthen this view. 

In many of these cases the pathological changes are simi- 
lar to those caused by infection. A marked fibrinous exu- 
date, for example, is as a rule caused by infection. In many 
of these cases this is the most conspicuous change. The vil- 
lous tufts on the synovial membrane are similar to those 
commonly occurring on the peritoneal or pleural surfaces. 
In the latter cavities they are thought to be due to bacterial 
irritation, so that in the joint they are possibly of an infec- 
tious nature. 

In many of the cases studied bacteria were found in the 
joints. In some they were obtained in pure culture, while in 
others there were mixed infections. In several instances 
where culture media inoculated from other organs of the 
body remained sterile, a growth was obtained from the joints. 



THE PATHOLOGY OF SPAVIN. 26 1 

The various bacteria isolated were B. coli, staphylococci, 
streptococci, an unidentified rod-shaped organism in one 
case, and Bact. pyogenes in one case in a cow with suppura- 
tive mastitis in addition to joint lesions. 

Lesions similar to most of those found in the cases studied 
were produced experimentally by Nathan. They were pro- 
duced in dogs by intravenous inoculations of hemolytic 
streptococci, pneumococci, and staphylococci, respectively. 
In this series all the organisms produced practically the same 
changes, so that the lesions are not those due to a specific 
cause. 

In a recent study of spontaneous chronic arthritis in swine, 
Sekiguchi and Irons found hemolytic streptococci in two, 
bacilli in nine, and a mixed infection of streptococci and 
bacilli in four cases. In two they found bacteria in smears, 
but not in culture, and in two they found no bacteria. They 
produced joint lesions in pigs by subcutaneous and intrave- 
nous inoculation of the organisms found. 

The experimental data seem to strengthen the belief that 
many of the cases studied were caused by infection. 

From a study of these cases the following conclusions 
seem justifiable : 

1. That there are very commonly found in horses and 
cattle low-grade polyarticular inflammations, leading to 
erosions and ankylosis. 

2. That in these cases the hock joints are the ones most 
often affected by the inflammations. 

3. That it is advisable to have the term spavin indicate 
any inflammation of the hock joint leading to ankylosis. 

4. That the origin of spavin may be in the joint proper 
as well as in the subchondral bone. 

5. That in many cases spavin is apparently caused by 
infection. 

6. That the primary seat of erosions and ankylosis may 
be in any of the intertarsal as well as the tarso-metatarsal 
joints. 



262 GOLDBERG. 

7. That the so-called " synovial fossae " are pathological 
erosions. 

8. That the so-called " synovial villi " are, in many cases 
at least, pathological outgrowths caused by mild irritation. 

9. That the so-called " lime points " in the articular 
cartilages are areas of necrosis in which calcification has 
taken place. 

10. That a periarticular ankylosis is, in some cases at 
least, due to an ossifying inflammation of the capsular liga- 
ment. 

11. That in the cases studied the osteoclasts do not play 
an important part in the rarefying ostitis. 

[The author wishes to take this opportunity to thank Prof. S. H. 
Burnett, under whose supervision this work was done, for his encourage- 
ment and helpful criticisms. I am also indebted to him for selecting this 
subject, and for the gross description of Cases 17 and 37.] 



THE PATHOLOGY OF SPAVIN. 263 

BIBLIOGRAPHY. 

Abraham, P. S. Arthritis Deformans in the Horse. Dublin, 1SS4. 

Aronsohn. Inaug. Diss. Giessen, 1893. 

Bartels. Viehzucht u. Thierheilk., 1S43, i (cited by Aronsohn). 

Biiche, Karl. Inaug. Diss. Hanover, 1912. 

Biirki. Archiv. fiir Thierheilk., 1905, xxxi, 241. 

Burnett, S. H. Outline of Lectures in Special Pathology. 1916, 53. 

Clark, H. C. Journ. Am. Med. Assoc, 1917, lxix, 2099. 

Cresswell, B. Journ. Anat. and Phys., 1S95 (cited by Schafer). 

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Eberlein. Monatsh. f. prakt. Thierheilk., 1898, ix, 49. 

Engel, Hans. Inaug. Diss. Berlin, 1902. 

Frohner. Spezielle Chirurgie fiir Tierarzte, 1905, 256. 

Gibson, Wm. A. Diseases of Horses. London, 1754, ii, 252. 

Goldberg, S. A. Cornell Veterinarian, 1915, v, 90; Am. Vet. Rev., 
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Gray, de. The Complete Horseman and Expert Farrier. 1639, 324. 

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Ki ueger. Archiv. f. Thierheilk., 1905, 295. 

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Rvini, Carlo. Delle Infirmitadi De'caualli, 1602, 314. 

Schafer, E. A. Microscopic Anatomy. 191 2. 

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Ward, A. R. Cornell Veterinarian, 1917, vii, 29. 

W'hilelocke. Sprains and Allied Injuries of Joints. 1910. 

Weichselbaum, A. Virch. Arch., 187S, lxxiii, 461. 

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Ziegler, E. Virch. Arch., 1878, lxxiii, 355. 



264 GOLDBERG. 

DESCRIPTION OF PLATES XI. AND XII. 

Plate XL, Fig. i. — Thickened area on articular cartilage with begin- 
ning erosion from the subchondral bone. Right tibial trochlear ridge. 
Case 5. x 29. 

A. Thickened area on articular cartilage. 

B. Normal articular cartilage. 

C. Degenerated articular cartilage. 

D. Beginning erosion of the articular cartilage by vascularization 

from the subchondral bone. 

E. Congested subchondral bone. 

Fig. 2. — Beginning erosions from subchondral bone. Medial ridge of 
trochlear right femur. Case 22. x 20. 
A. Articular cartilage. 
B Areas where cartilage is being dissolved by fibrin and blood 

vessels. 
C. Rarefied subchondral bone. 
Fig. 3. — Erosion originating in the joint. Left astragalar trochlea. 
Case 35. x 20. 

A. Area where cartilage is absent. 

B. Fibrillation of the remaining articular cartilage. 

C. Subchondral bone apparently normal. 

Fig. 4. — Calcified area of necrosis in the articular cartilage tibio- 
astragalar articulation. Case 57. x 40. 

A. Calcified area of necrosis. 

B. Degenerated articular cartilage. 

C. Articular cartilage nearly normal. 

D. Subchondral bone denser than normal. 

Fig. 5. — Erosion originating in the joint. Right tibial trochlear ridge. 
Case 49. x 20. 

A. Area where cartilage is gone. 

B. Remaining articular cartilage. 

C. Pinkish staining homogeneous material in place of cartilage. 

D. Normal subchondral bone. 

Plate XII., Fig. 6. — Organizing fibrin on right patella. Case 22. 

X2 5 . 

A. Subchondral bone. 

B. Articular cartilage. 

C. Fibrous connective tissue. 

D. Granulation tissue. 

E. Fibrin. 

Fig. 7. — Adhesions of different parts of the synovial membrane. Left 
patellar articulation. Case 16. 9/10 natural size. 

A. Patellar articular surface. 

B. Arborous film of blood vessels on the articular cartilage. 

C. Band of connective tissue forming an adhesion between several 

parts of the synovial membrane and the patellar articular 
surface. 



THE PATHOLOGY OF SPAVIN. 265 

D. Filliform and papilliform villous tufts on the synovial mem- 

brane. 

E. Accessory cartilage of the patella. 

F. Thickened capsular ligament. 

Fig. S. — Fibrous ankylosis that apparently began in the joint. Right 
calcaneo-astragalar articulation. Case 41. x 30. 

A. Remaining cartilages on both articular surfaces. 

B. Embryonal connective tissue and blood vessels in the joint 

sinus. 

C. Subchondral bones. 

Fig. 9. — Ossification in an organized fibrinous exudate on synovial 
membrane. Right stifle. Case 22. x 35. 

A. Island of bone. 

B. Granulation tissue. 

Fig. 10. — Enlarged Haversian canal. Left third tarsus. Case 37. 
x 250. 

A. Bony lamellae. 

B. Osteoblasts lining the Haversian canal. 

C. Haversian canal containing fibrin and fibroblasts. 

Fig. 11. — Fibrous ankylosis in the articulation between the astragalus 
and central tarsus right hock. Case 41. x 75. 

A. Articular cartilage nearly normal. 

B. Fibroblasts and blood vessels producing ankylosis of the joint. 

C. Proliferating fibrocartilage in the ankylosis. 

D. Formation of bone in the ankylosis. 

E. Enlarged Haversian canals containing fibrin, fibroblasts, and 

congested blood vessels, and lined by osteoblasts. 

F. Degenerated articular cartilage. 

G. Exudate of fibrin in the joint sinus. 



The Journal of Medical Research, Vol. XXXVIII., No. 2, May, 191S. 



Journal of Medical Research. 



Vol. XXXVIII. Plate XI 






HI 















. D . >• ■.- 







Goldberg. 



Spavin. 



Journal of Medical Research. 



Vol. XXXVIII. Plate XII 




Coldberg. 



Spavin. 



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